Living animals have an immune system which protects them against the introduction and advancement of pathogenic microorganisms. Upon detection of an antigen, such as a pathogenic microorganism, T cells are activated to produce lymphokines that influence the activities of other host cells while B cells are stimulated to mature and produce immunoglobulins or antibodies that react with the antigen.
The effectiveness of the immune system depends upon several factors including the specific pathogenic microorganism and the vitality of the immune system. Certain pathogenic microorganism are capable of reducing immune system activity while others are capable of overcoming the normal responsiveness of the system.
Immune senescence is a decrease in the antibody responsiveness of the immune system which retards the ability of the system to immunize the body against pathogenic microorganisms. Such a depressed immune system results in an increase in the frequency and severity of pathogenically induced maladies and possibly death.
Immune senescence may result as a natural consequence of aging or as a deleterious effect of pathological microorganism(s). Immune senescence is one of the major health problems of our time with a general consensus and within the medical profession that the problem may soon reach epidemic proportions.
Loria et al. (U.S. Pat. No. 5,077,284) discloses that administration of dehydroepiandrosterone (DHEA) (.DELTA.5-Androstene-3-ol-17-one) can improve a host's response to viral infections. Unfortunately, DHEA also stimulates the production of sex hormones to such an extent that it is generally considered unsuitable for use as a therapeutic agent. The Loria et al. patent itself acknowledges this drawback at column 2, lines 21-27. Loria et al. attempts to dismiss this drawback by suggesting that the side effect may be overcome by monitoring the dose and/or using analogs. Unfortunately, others have been unable to overcome the side effect by the methods suggested by Loria et al. and Loria et al. does not suggest any specific dosage manipulations or analogs which could be used.
It is widely recognized that steroid hormones exhibit "structurally specific" activity such that minor changes in structure, including the addition, deletion and/or substitution of single substituent groups, frequently alters the biological activity of the steroid. See, Ortho Pharmaceutical Corp. v. Smith, 959 F.2d 936, 943, 22 U.S.P.Q.2d 1119, 1125 (Fed. Cir. 1992). Adjacent steroid homologs cannot be presumed to possess the same utility due to the greater unpredictability of compounds in that field. Brenner v. Manson, 383 U.S. 519, 532, 148 U.S.P.Q. 689, 694 (1966). Essentially identical structures are generally required before one skilled in the art would be inclined to believe that two steroids would possess the same properties or characteristics.
This "structurally specific" activity of steroids has frustrated attempts to locate a derivative of DHEA which exhibits the desired biological response without the undesired side effects.
Accordingly, a substantial need exists for a therapeutic agent effective for enhancing the responsiveness of the immune system against the invasion of pathological microorganisms.